Thus, our data demonstrated that the downstream target of AR silencing, CCL2, plays key roles to mediate THP-1 migration as well as PCa cell migration, and interruption of the CCL2/CCR2S/STAT3 axis with either anti-CCL2 antibody, CCR2 antagonist, or STAT3 inhibitor suppressed AR silencing-induced PCa cell migration and EMT induction. This evidence concerns the gene STAT3 and posterior cortical atrophy.